LepR

mutations result in elevated circulating leptin, but the brain cannot respond

to the signal, whereas Congenital Leptin Deficiency involves no circulating

leptin.

LepR mutations result in very low or absent circulating leptin levels. 

LepR mutations cause late-onset obesity that only appears after age 40.

Genetic

ablation of AgRP neurons in adult mice leads to profound hyperphagia and morbid

obesity.

Glutamate is the primary orexigenic signal released by NPY cells to provide rapid control of feeding. 

POMC neurons produce α-MSH which stimulates food intake by activating MC4R. 

AgRP/NPY neurons are potent orexigens that increase food intake and can directly inhibit POMC neurons via GABAergic projections. 

CCK

reduces food intake exclusively through actions on vagal afferent fibres

signalling to the NTS, unlike GLP-1 which can act directly on neurons in the

hypothalamus.

CCK

levels peak 6 hours after a meal, whereas PYY and GLP-1 levels peak within 15

minutes.

CCK

crosses the blood-brain barrier directly to act on the PVN, whereas PYY acts

only on the Area Postrema.

CCK

is secreted from L-cells in the rectum, while PYY is secreted from I-cells in

the duodenum.

They

prevent the body from entering the "fasted state"

neuroendocrinological profile.

They

may increase fullness/satiety and promote greater weight loss compared to

non-ketogenic high-protein diets in the short term.

They

work by increasing the hepatic absorption of fat.

They

provide an unlimited supply of glucose to the brain to prevent hunger.

It acts as a norepinephrine-dopamine reuptake inhibitor to stimulate the reward pathway and address the "Emotional Hunger" phenotype. 

It

serves as an MC4 receptor antagonist to block the β-endorphin-mediated inhibition of the brain's

satiety centres.

It

triggers a peripheral uncoupling of mitochondrial oxidative phosphorylation,

allowing for energy dissipation as heat without central nervous system

involvement.

It

provides direct stimulation to anorexigenic POMC neurons while utilising

GABAergic signalling to indirectly inhibit orexigenic NPY/AgRP neurons.

Ghrelin

acts as an endogenous antagonist at the MC4R to block the satiety effects of

-MSH during fasting; its lack of a role in the fed state is due to the

competitive binding of PYY 3-36 to the same receptor.

Ghrelin

utilizes fenestrated capillaries to act exclusively on the ventromedial

hypothalamus (VMH) to inhibit the "satiety center" during periods of

negative energy balance; it lacks a role in the fed state because tanycytes

form a physical barrier that prevents its entry into the hypothalamus when

plasma glucose is elevated.

Ghrelin

binds to the GHSR (Growth hormone secretagogue receptor) on POMC neurons to

stimulate the release of -endorphin as a fasting signal; it has no functional

role in the fed state because its secretion is inhibited.

Ghrelin

coordinates the hypothalamic response to fasting by activating the GHSR on

AgRP/NPY neurons to drive hunger and GABAergic inhibition of POMC activity;

this orexigenic circuit lacks a functional role in the fed state because

ghrelin levels are rapidly suppressed by nutrient ingestion.

Flip the images 90 degrees so they looked more anatomically correct

Use a software program to change the fluorescently labelled immune cells from green to red, so that the colour is different to the apoptotic cells

Use a software program to remove any fluorescently labelled cells that are not immune cells or cells undergoing apoptosis

Eliminate all data collected from an animal because the level of airway disease was significantly less than normal

Ghrelin

acts as a competitive antagonist at the MC4R in the paraventricular nucleus,

preventing -MSH from binding and thereby inducing a rapid "stop-eat"

signal.

Ghrelin

directly activates the GHSR on AgRP/NPY neurons to provide an orexigenic drive

while simultaneously utilising GABAergic projections to inhibit the

anorexigenic activity of POMC neurons.

Ghrelin

binds to the GHSR (Growth hormone secretagogue receptor) on POMC neurons to

stimulate the release of -endorphin, which serves as a "brake" on

energy expenditure.

Ghrelin

bypasses the arcuate nucleus via fenestrated capillaries to act exclusively on

the ventromedial hypothalamus (VMH), where it inhibits the "satiety

centre" to prevent the feeling of fullness.

It

acts as a primary incretin, facilitating glucose-stimulated insulin release

from the pancreas.

Its

circulating levels are significantly elevated in obese individuals,

contributing to "satiety resistance."

It

is found in highest concentrations in the duodenum and jejunum to provide

early-phase meal termination signals.

It

is secreted in the active form PYY 3-36 and acts specifically via Y2 receptors

located only on orexigenic NPY/AgRP neurons in the ARC.

Severe early-onset obesity, adrenal insufficiency (due to ACTH deficiency), and red hair pigmentation. 

Starvation,

death, and inability to produce NPY.

Increased energy expenditure, hyperphagia, and dark skin pigmentation